MINI REVIEW
published: 15 May 2019
Edited by:
Marion Leboyer,
Université Paris-Est Créteil
Val de Marne,
France
Reviewed by:
Kurt Leroy Hoffman,
Autonomous University of Tlaxcala,
Mexico
Yilang Tang,
Emory University,
United States
*Correspondence:
Joseph Firth
J.Firth@Westernsydney.edu.au
Specialty section:
This article was submitted to
Molecular Psychiatry,
a section of the journal
Frontiers in Psychiatry
Received: 17 December 2018
Accepted: 03 May 2019
Published: 15 May 2019
Citation:
Firth J, Veronese N, Cotter J,
Shivappa N, Hebert JR, Ee C, Smith L,
Stubbs B, Jackson SE and Sarris J
(2019) What Is the Role of Dietary
Inflammation in Severe Mental
Illness? A Review of Observational
and Experimental Findings.
Front. Psychiatry 10:350.
doi: 10.3389/fpsyt.2019.00350
Frontiers in Psychiatry  |  www.frontiersin.org
doi: 10.3389/fpsyt.2019.00350
What Is the Role of Dietary
Inflammation in Severe Mental
Illness? A Review of Observational
and Experimental Findings
Joseph Firth 1,2*, Nicola Veronese 3,4, Jack Cotter 5, Nitin Shivappa 6,7,8, James R. Hebert 6,7,8,
Carolyn Ee 1, Lee Smith 9, Brendon Stubbs 10,11, Sarah E. Jackson 12 and Jerome Sarris 1,13
1 NICM Health Research Institute, Western Sydney University, Westmead, NSW, Australia, 2 Division of Psychology and
Mental Health, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, United Kingdom, 3 Laboratory
of Nutritional Biochemistry, Research Hospital, IRCCS “S. de Bellis”, Castellana Grotte, Italy, 4 Aging Branch, Neuroscience
Institute, National Research Council, Padua, Italy, 5 Cambridge Cognition, Cambridge, United Kingdom, 6 Cancer Prevention
and Control Program, Arnold School of Public Health, University of South Carolina, Columbia, SC, United States, 7 Department
of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, United States,
8 Connecting Health Innovations LLC, Columbia, SC, United States, 9 Cambridge Centre for Sport and Exercise Sciences,
Anglia Ruskin University, Cambridge, United Kingdom, 10 Physiotherapy Department, South London and Maudsley NHS
Foundation Trust, London, United Kingdom, 11 Health Service and Population Research Department, Institute of Psychiatry,
Psychology and Neuroscience, King’s College London, London, United Kingdom, 12 Department of Behavioural Science
and Health, University College London, London, United Kingdom, 13 Department of Psychiatry, University of Melbourne,
The Melbourne Clinic Professorial Unit, Melbourne, VIC, Australia
Severe mental illnesses (SMI), including major depressive disorder, bipolar disorder, and
schizophrenia, are associated with increased inflammation. Given diet’s role in modulating
inflammatory processes, excessive calorie-dense, nutrient-deficient processed food
intake may contribute toward the heightened inflammation observed in SMI. This review
assesses the evidence from observational and experimental studies to investigate how
diet may affect physical and mental health outcomes in SMI through inflammation-
related pathways. Cross-sectional studies indicate that individuals with SMI, particularly
schizophrenia, consume more pro-inflammatory foods and fewer anti-inflammatory
nutrients than the general population. Cohort studies indicate that high levels of dietary
inflammation are associated with increased risk of developing depression, but there is
currently a lack of evidence for schizophrenia or bipolar disorder. Randomized controlled
trials show that dietary interventions improve symptoms of depression, but none have
tested the extent to which these benefits are due to changes in inflammation. This review
summarizes evidence on dietary inflammation in SMI, explores the directionality of these
links, and discusses the potential use of targeted nutritional interventions for improving
psychological well-being and physical health outcomes in SMI. Establishing the extent to
which diet explains elevated levels of inflammatory markers observed in SMI is a priority
for future research.
Keywords: nutrition, schizophrenia, bipolar disorder, nutrients, vitamin
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Firth et al.
INTRODUCTION AND AIMS
Recent meta-analyses have confirmed that severe mental
illnesses (SMI), including major depressive disorder (MDD),
bipolar disorder, and schizophrenia, are associated with increased
levels of both peripheral inflammatory markers (1) and systemic
inflammation (2). Additionally, heightened inflammation could
present a novel treatment target for MDD, given that the anti-
depressant efficacy of various pharmacological and lifestyle
interventions appears to be associated with reductions in
inflammation (3, 4). In schizophrenia, the evidence for
antipsychotics altering inflammatory markers is mixed (1, 5),
although there is some preliminary evidence to indicate that
various adjunctive interventions may confer beneficial effects
through reducing inflammatory status (6, 7).
Calorie-dense diets that are high in saturated fats and simple
carbohydrates appear to increase peripheral inflammatory markers,
whereas diets high in fiber and vegetables reduce inflammation
(8–12). Systematic reviews of dietary patterns in people with
SMI have shown elevated intakes of sugar-sweetened soft drinks,
refined grains, and processed meat are common in this population
(13, 14). However, the degree to which these dietary patterns
heighten inflammation in SMI, and the potential impact on
physical and mental health outcomes, is relatively unexplored. This
comprehensive review brings together the evidence from cross-
sectional, longitudinal, and experimental studies on this topic to:
(i) Examine the extent to which inflammatory potential of
the diet (hereafter referred to as “dietary inflammation”) is
elevated in SMI populations;
(ii) Explore the directionality of the links between dietary
inflammation and symptoms of SMI;
FIGURE 1 | Dietary Inflammatory Index (DII) scores from 53,270 healthy controls, compared to major depressive disorder (MDD) (n = 14,422), bipolar disorders
(BPD, n = 933), and schizophrenia (SZ, n = 254). Midpoint shows adjusted means. Error bars show 95% confidence intervals. *Statistically significant difference
compared to healthy controls. Data derived from Firth et al. (15).
Frontiers in Psychiatry  |  www.frontiersin.org
Dietary Inflammation in Severe Mental Illness
(iii) Discuss the existing evidence for the use of nutritional
interventions for improving health outcomes in SMI and
how these effects may act through inflammatory pathways.
FOOD INTAKE AND DIETARY
INFLAMMATION IN PEOPLE WITH
SEVERE MENTAL ILLNESSES
A recent large-scale study of the UK Biobank (15) compared the
macro- and micro-nutrient intake of individuals with diagnosed
MDD (n = 14,619), bipolar disorder (n = 952), and schizophrenia
(n = 262) to healthy controls (n = 54,010), showing that people
with SMI consumed significantly more carbohydrate, sugar, fat,
and saturated fat than healthy controls (all p < 0.001), even when
controlling for age, gender, education, BMI, social deprivation,
and ethnicity. The study also examined the inflammatory
potential of food intakes of individuals with SMI compared with
the general population using the “Dietary Inflammatory Index”
(DII®). The DII is a literature-derived, population-based measure,
which provides an estimate of the inflammatory potential of an
individual’s diet from up to 45 individual food parameters (16).
DII scores have been validated against various blood markers of
inflammatory status across a number of different populations
(17–21). The DII scores in SMI samples in the UK Biobank are
displayed in Figure 1 [derived from Firth et al. (15)], adjusted
for age, gender, and total energy intake. These data show highly
elevated dietary inflammation in individuals with schizophrenia,
along with smaller, but significantly increased, levels of dietary
inflammation in individuals with MDD (all p < 0.01). Although
dietary inflammation in the bipolar disorder group was similarly
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Firth et al.
larger than healthy controls (p = 0.03), this difference was
reduced to a marginally non-significant trend after adjusting for
BMI and socioeconomic status (p = 0.07).
It is interesting to note that despite the vast number of studies
examining elevated levels of peripheral inflammation observed
across all classes of SMI (1), none have accurately controlled for the
potential confounding factor of diet. Furthermore, a priority for
future research is to validate the accuracy of dietary reporting in SMI.
Interestingly, previous research comparing other lifestyle factors
(i.e., physical activity) using objective against self-report measures
in SMI have shown that people with schizophrenia significantly
overestimate health behaviors compared with the general population
(22). Therefore, replication of these findings, using validated
measures in SMI alongside blood markers of inflammation, is
required to establish how diet may relate to inflammation in SMI.
Along with poor mental health, people with SMI experience
drastic inequalities in physical health, including elevated rates
of obesity, diabetes, and cardiometabolic disorders, ultimately
contributing to a reduced life expectancy of around 20 years
(23). Given the clear causal links between dietary inflammation
and these health outcomes established in the general population
(10–12), and the established benefits of dietary interventions for
physical health in SMI (24), it is reasonable to explore dietary
inflammation as one risk factor driving some of the physical health
inequalities observed in this population. Indeed, the highest levels
of dietary inflammation are observed in schizophrenia: a group that
also experiences significantly worse physical health outcomes than
other classes of SMI (25, 26). Poor dietary quality associated with
schizophrenia may even be driven by side effects of antipsychotic
medications, which may increase appetite through interfering with
the “hunger hormone,” ghrelin (27). Clearly, there is an urgent need
for future research to determine the mechanisms through which
poor diet may be driving adverse health outcomes in people with
SMI. This line of investigation will provide novel insights into
the etiology of the physical health inequalities observed in this
population and has the potential to inform clinical care.
A key limitation of the current literature is a lack of large-scale
data on dietary patterns among young people with SMI, thus
making it difficult to determine whether poor diet precedes the
onset of mental illness, or vice versa. In the general population, data
suggest that younger people tend to have worse diets than older
adults (28). This also may apply to SMI populations, as nutritional
deficits in psychosis are evident even prior to antipsychotic
treatment (29). Thus, in the following section, we review the
prospective studies examining links between high levels of dietary
inflammation and the subsequent onset of mental illness.
PROSPECTIVE ASSOCIATIONS
BETWEEN DIETARY INFLAMMATION
AND PSYCHIATRIC SYMPTOMS
Poor nutrition has been implicated in the onset and persistence of
psychiatric disorders (30). In general, cohort studies have shown
that dietary patterns, such as a Mediterranean diet, which is rich
in fruits, vegetables, olive oil, and legumes, may be protective
against mental health disorders (31–38). By contrast, increased
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Dietary Inflammation in Severe Mental Illness
risk of mental disorders has been observed with dietary patterns,
such as the Western diet, characterized by high intake of saturated
fat and refined carbohydrates (33, 39–41).
Inflammation presents one feasible mechanism through
which diet may affect the risk of mental disorders. This is
supported by multiple cohort studies showing that higher DII
scores are associated with increased risk of depression (42–49).
Combining all longitudinal data on this topic (including 77,420
participants from seven different studies), a recent meta-analysis
confirmed that higher levels of dietary inflammation were
associated with 31% increased risk of depression over the 5- to
13-year follow-up period (50). This meta-analysis also found
that pro-inflammatory diets were more strongly associated with
depression among females than males (50), although significant
relationships were observed for both sexes.
Despite these positive findings on links between depression
and dietary inflammation calculated from self-report measures,
future research must establish if these relationships are mediated
by biological markers of inflammatory status. Although a
number of studies have found joint relationships between
dietary inflammation, inflammatory markers, and depressive
symptoms (51–53), those findings are inconsistent with other
results showing that dietary patterns associated with heightened
inflammatory markers do not consistently predict depression
scores (54).
Currently, there is an urgent need for longitudinal studies to
assess how dietary inflammation is related to the onset of other
classes of SMI, because there is currently no strong evidence
linking dietary inflammation with risk of bipolar disorder or
schizophrenia. As the effects of dietary inflammation on mental
health are also observed in adolescence (51), when the majority
of SMIs first arise (55), the potential impact that this may have
on risk of bipolar and psychotic disorders is worthy of further
examination.
Along with clinical symptoms, people with SMI (and
particularly schizophrenia) also display a range of cognitive
deficits (56–58), which impede daily functioning (59, 60), and
are not treated by psychotropic medications (61, 62). There
is an emerging literature suggesting that elevated peripheral
inflammatory markers are associated with deficits in cognitive
function among patients with psychiatric disorders (1, 63).
Though the specific mechanisms underlying this association
remain unclear, chronic and acute inflammation is thought to
have a number of detrimental effects on brain structure and
function, which, in turn, appear to adversely affect cognitive
performance (64–66).
Poor diet and obesity also have a well-established link with
cognitive dysfunction (67, 68). There is mounting evidence
that these associations may be mediated by inflammatory
processes (69), suggesting that diet has the potential to act as a
modifiable risk factor for cognitive dysfunction both in clinical
and non-clinical populations. Much of the work investigating
the association between diet, inflammation, and cognition has
come from a series of cross-sectional and longitudinal studies in
older adults, which indicate that diets with high inflammatory
potential may be associated with accelerated cognitive decline
and reduced brain volume (70–72). Considering the high levels
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Firth et al.
of dietary inflammation and cognitive deficits observed in SMI,
along with indicated relationships between cognitive functioning
and diet in other populations, this area presents a promising
avenue for future research (73).
EXPERIMENTAL MANIPULATION OF
DIETARY INFLAMMATION: CAN WE MAKE
A DIFFERENCE TO MENTAL HEALTH?
A recent meta-analysis examined the effects of dietary
interventions on mental health in 16 randomized controlled
trials (RCTs) of 45,826 participants (74). Dietary improvement
significantly reduced symptoms of depression [g = 0.275; 95%
confidence interval (CI), 0.10–0.45; p = 0.002], with no changes
in anxiety observed. Interestingly, similar degrees of benefit for
depressive symptoms were observed from all the different dietary
approaches trialed; dietary interventions primarily designed
to improve nutrition [e.g., the Mediterranean diet, which is
typically linked with anti-inflammatory effects (11)] were no
more beneficial for mental health than those aimed at reducing
bodyweight or decreasing dietary fat intake (74). This may be
because, even without increasing anti-inflammatory nutrient
intake, weight-loss and changes in energy balance can reduce
inflammation through reducing excess adipose tissue, which is
associated with heightened inflammation (75, 76).
However, 15 of the 16 RCTs in this meta-analysis only
examined effects on depressive symptoms in samples with “sub-
clinical” depression (i.e., samples without a confirmed diagnosis of
MDD). However, the single trial conducted in clinically depressed
participants (75) observed large reductions in depressive
symptoms from a 12-week modified Mediterranean diet, with
32.3% of participants achieving remission from the dietary
intervention versus 8.0% in the social support control condition
(p = 0.028). Subsequent RCTs have replicated these findings of the
Mediterranean diet reducing symptoms in people with moderate
to severe depression (76). As a meta-analysis of 50 studies (10) has
shown, the Mediterranean diet significantly reduces inflammatory
markers in other (i.e., non-psychiatric) populations, and it is
possible that the benefits in people with depression are linked
to the anti-inflammatory effects. However, this has yet to be
assessed, as no studies have measured changes in inflammation
following dietary interventions in depression. Furthermore, there
is currently no experimental evidence showing beneficial effects
of dietary interventions on inflammation and mental health in
schizophrenia or bipolar disorder.
Nonetheless, RCTs of individual nutrient-based supplements
(nutraceuticals) have provided valuable insights into how nutrition
can influence mental health in SMI through inflammatory
pathways. For instance, in an RCT of 155 individuals with MDD,
Rapaport et al. (77) found that patients with baseline elevated
markers of inflammation were significantly more responsive to
omega-3 treatment (mediated, in principle, via eicosapentenoic
acid) (78). The antidepressant effects of omega-3 fatty acids
working through the reduction of inflammation also were
implicated in a seminal study by Su (79). This study examined
depression in people with hepatitis C, undergoing interferon
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Dietary Inflammation in Severe Mental Illness
(IFN) alpha therapy, which commonly induces depressive
symptoms due to its inflammatory effects (80). However, Su
et al. (79) found that omega-3 supplementation reduced the
risk of developing depression following INF-a treatment.
Other nutrients, such as folate, have also been found to reduce
depression in people with high levels of inflammation (81), again
indicating these adjunctive treatments may confer symptomatic
benefits through inflammatory pathways.
Beyond MDD, there are preliminary data from RCTs
suggesting that anti-inflammatory nutrients, such as omega-3
and folate-based compounds, may also be effective for other
SMIs, including bipolar disorder and schizophrenia (82). Because
inflammation is particularly elevated during onset of psychotic
disorders, these adjunctive treatments may have neuroprotective
effects in the early stages of illness among young people (83, 84),
potentially improving cognitive outcomes for some patients.
However, the extent to which their effects are due specifically to
their anti-inflammatory properties is not fully ascertained.
CONCLUSIONS AND FUTURE RESEARCH
The current evidence from human studies examining the role
of dietary inflammation in SMI are shown in Figure 2. The
cross-sectional literature provides consistent evidence that
individuals with SMI consume more pro-inflammatory foods
than the general population, and fewer anti-inflammatory
nutrients—which may contribute toward the heightened levels
of inflammatory markers observed in SMI. In the few studies
that have compared different classes of SMI, the highest dietary
risks are observed among people with schizophrenia (who also
have the most severe disparities in physical health, compared
with other mental disorders). However, the bulk of both the
observational and experimental studies examining the links
between dietary inflammation and mental health have been
conducted in depression (see Figure 2A)—with a relative
dearth of evidence in other disorders. Therefore, there is now
a need for researchers and clinicians to build upon the existing
evidence in MDD and give further attention to the impact of
dietary inflammation in schizophrenia and bipolar disorder
and explore the potential benefits of dietary modification for
these populations.
The longitudinal studies now provide population-scale data
showing that high levels of dietary inflammation are associated
with increased the likelihood of developing depression over
time. However, there is little evidence to suggest that this also
applies to schizophrenia or bipolar disorder. Alongside this, a key
remaining question in this field (which can only be addressed
by experimental studies), is: “Can reducing dietary inflammation
make a difference?” or, more specifically, “Is it possible that
dietary modification can reduce inflammation and thus improve
symptoms in people with SMI?”
Currently, there is no experimental evidence to show that
a specific “anti-inflammatory” diet influences psychiatric
symptoms of schizophrenia or bipolar disorder. Furthermore,
whereas RCTs and meta-analyses have recently shown that
dietary improvement reduces symptoms of depression (in both
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Firth et al. Dietary Inflammation in Severe Mental Illness

FIGURE 2 | Key Findings and Future Questions: A map of the evidence for the role of dietary inflammation in severe mental illnesses (SMI), with regard to (A)
different conditions, and (B) different aspects of the interaction between dietary inflammation, inflammatory markers, and psychiatric disorders.

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Firth et al.
clinical and non-clinical populations), the extent to which this
is due to anti-inflammatory effects of dietary interventions
has not been assessed. Nonetheless, some evidence from
nutraceutical trials suggests that certain anti-inflammatory
nutrients may provide adjunctive treatments for subgroups of
individuals with mental health conditions with particularly
elevated levels of inflammation.
With regard to whole-diet interventions, it is interesting to
consider the prevalent finding that the weight loss, fat reduction,
or Mediterranean diets trialed so far all appear to confer similar
beneficial effects on depressive symptoms. Whereas this may
indicate a lack of specificity, it should be acknowledged that
each of these interventions, although differing in stated aims,
generally have some key factors in common. Specifically, all of
these interventions generally involve decreasing the amount of
refined, processed calorie-dense foods, while increasing intake
of nutrient-dense natural-occurring fiber and vegetables.
Therefore, the general equivalence across difference types
of diets could ultimately produce an encouraging message,
suggesting that highly specific or specialized diets are perhaps
unnecessary for the average individuals, as adhering to very
simple and universally accepted dietary advice appears to be
equally beneficial for psychological well-being—and sufficient
for avoiding the potentially deleterious effects on mental health
of a “junk food” diet. To provide greater insight on this, future
research should attempt to elucidate the specific mechanisms
through which the dietary impacts upon inflammation to
influence mental health. For instance, hyperglycemia and
hyperinsulinemia after a meal of refined starches and sugars
may promote inflammation by increasing production of free
radicals and pro inflammatory cytokines (85, 86), whereas
high levels of saturated fat intake decrease production of
short chain fatty acids such as butyrate, which have anti-
inflammatory properties (87). Alongside these nutritional
factors, obesity and excess adipose tissue themselves directly
heighten inflammation—suggesting that attenuating these
adverse states of health through calorie restriction and low-
fat diets could reduce inflammatory status and thus improve
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Conflict of Interest Statement: JC is an employee of Cambridge Cognition Ltd.
JH owns controlling interest in Connecting Health Innovations LLC (CHI), a
company planning to license the right to his invention of the Dietary Inflammatory
Index (DII®) from the University of South Carolina in order to develop computer
and smart phone applications for patient counseling and dietary intervention
in clinical settings. NS is an employee of CHI. The subject matter of this paper
will not have any direct bearing on that work, nor has that activity exerted any
influence on this paper. JF is supported by a Blackmores Institute Fellowship. JF,
JS, and CE declare that as a medical research institute, NICM Health Research
Institute receives research grants and donations from foundations, universities,
government agencies, and industry. Sponsors and donors provide untied and tied
funding for work to advance the vision and mission of the Institute. CE declares
that she is an integrative GP. The remaining authors declare that the research was
conducted in the absence of any commercial or financial relationships that could
be construed as a potential conflict of interest.
Copyright © 2019 Firth, Veronese, Cotter, Shivappa, Hebert, Ee, Smith, Stubbs,
Jackson and Sarris. This is an open-access article distributed under the terms of
the Creative Commons Attribution License (CC BY). The use, distribution or
reproduction in other forums is permitted, provided the original author(s) and the
copyright owner(s) are credited and that the original publication in this journal
is cited, in accordance with accepted academic practice. No use, distribution or
reproduction is permitted which does not comply with these terms.
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